Racial Inequalities in Drinking Water Lead Exposure: A Wake-Up Call to Protect Patients with End Stage Kidney Disease

Chronic lead exposure in public drinking water remains a persistent environmental injustice that disproportionately affects Black communities across the United States. In this issue of JASN, Danzinger et al.¹ evaluated the association of public drinking water lead exposures with serum hemoglobin levels and use of erythropoietin stimulating agent in a national registry of patients with ESKD. Adult Black patients with ESKD were exposed to higher levels of lead in public drinking water than White patients, and higher public water lead exposure was associated with more severe kidney disease. This unacceptable inequality in public drinking water lead exposure by race/ethnicity among patients with ESKD is, unfortunately, not surprising. Disparities in water lead exposure reflect the same structural environmental racism responsible for disparities in child blood lead levels, which have persisted for decades.²

Lead exposure disparities persist, in part, because of inadequacies and injustices in the major lead reduction drinking water regulation of the twentieth century: the US Environmental Protection Agency Lead and Copper Rule (LCR). Despite substantial epidemiologic and toxicologic evidence establishing a causal link between lead exposure and child neurodevelopment, numerous health effects among adults including CKD,^3,4 and no safe level of lead exposure, the LCR has failed to adequately and justly reduce drinking water lead. Others have described these inadequacies in detail.^5,6

Danzinger et al.¹ extracted medical records for nearly 600,000 patients with ESKD and assigned them drinking water lead exposures on the basis of over 200,000 compliance records reported by public water systems in accordance with the LCR. Black patients were served by water systems that reported both higher 90th percentile lead concentrations and smaller declines in 90th percentile lead concentrations over time compared with White patients. Across all patients served by water systems with detectable 90th percentile lead concentrations, a water lead increase of 0.01 mg/L was associated with significant reductions in pre-ESKD hemoglobin concentrations (−0.02 g/dl; 95% confidence interval, −0.01 to −0.2 g/dl) and higher erythropoietin stimulating agent use (0.4%; 95% confidence interval, 0.2% to 0.6%). Water lead exposure was also associated with renal anemia even at water lead concentrations below the current LCR action level of 0.015 mg/L. Compared with patients served by water systems with a 90th percentile lead concentration <0.001 mg/L, patients served by water systems with a 90th percentile lead concentration between 0.0075 and 0.015 mg/L experienced significantly lower pre-ESKD hemoglobin and higher erythropoietin stimulating agent use. Although these effect estimates may seem small, the clinical and public health effects are likely to be substantial when applied across the entire United States population.

Nephrologists and other readers of JASN must take note of these findings to address environmental injustices in lead exposure and their effects on patients with ESKD. First, inequalities in drinking water lead exposure persist in United States adults and are clinically relevant. Because the majority of lead is stored in bone with a half-life of decades, even childhood exposure disparities remain relevant for the development and severity of adult chronic disease.⁷ Disaggregating clinical and epidemiologic data, as Danzinger et al.¹ have done, is critical so that clinical and public health interventions and regulatory action can be immediately directed toward the most highly exposed communities.

Second, these findings add to a growing body of evidence highlighting the relevance of low-level lead exposure for adult chronic disease, including CKD. The epidemiologic, toxicologic, clinical, and experimental evidence now exists to categorize lead as a cardiovascular risk factor.⁴ Additional prospective epidemiologic studies at current low levels of lead exposure are needed to advance similar research for CKD. This study, however, clearly supports that among patients with ESKD, lead exposure significantly affects other systems and is associated with clinically relevant outcomes. Additional studies are needed to determine if chronic, low-level lead exposure is associated with other metrics of CKD severity or other complications associated with CKD. Future epidemiologic work focused on adult lead exposure can utilize publicly available water lead compliance records in the Safe Drinking Water Information System (SDWIS), as Danzinger et al.¹ have done, to study the contribution of lead exposure to the current CKD epidemic. Other studies using lead biomarkers to assess exposure are also needed. In the first Trial to Assess Chelation Therapy, repeated chelation with EDTA reduced the relative risk of a composite cardiovascular outcome by 52% among patients with diabetes.⁸ This exceptional benefit was unanticipated, but it underscores the major clinical relevance of chronic, low-level metal exposures common in the United States population. Other clinical benefits of EDTA, beyond cardiovascular disease, should be investigated, especially in light of these new findings, which indicate that public water lead exposure is associated with renal anemia in patients with ESKD.

Third, estimating drinking water lead exposure for epidemiologic purposes is extremely difficult, especially at the national scale, because current publicly available LCR monitoring data in SDWIS only report water system 90th percentile concentrations (from a targeted sampling of taps across the distribution system) when they exceed the lead action level (15 ppb), instead of reporting sampled concentration values.⁵ Improvements in LCR sampling and public reporting requirements are urgently needed to improve water lead exposure estimates, which can in turn enable the identification of inequalities in water lead exposure at a finer geographic resolution and the epidemiologic study of water lead exposure and adverse health outcomes.

Finally, the current LCR is inadequately protective of human health. Nephrologists, pediatricians, epidemiologists, and other health professionals and public health scientists must advocate for the complete elimination of lead in drinking water. The findings by Danzinger et al.¹ come at a critical time for informing nationwide drinking water regulation changes and infrastructure investments. Many experts have previously described the significant economic and public health benefits to eliminating leaded service lines and pipes across the United States.⁹ Efforts to replace leaded infrastructure should target the most highly lead-exposed populations, including low-income communities, Black communities, and rural communities reliant on unregulated private wells. Infrastructure investments should also include additional financial support for water systems serving small, rural, and tribal communities—the same communities disproportionately exposed to other drinking water contaminants, such as arsenic and nitrates.

Over the last several decades, public health policies and regulatory actions successfully reduced nationwide child blood lead levels by regulating lead in gasoline emissions, food cans, paint, household dust, and to some extent, public drinking water (Figure 1).¹⁰ These regulatory actions dramatically reduced the amount of lead inhaled or ingested, and as a result, the nationwide geometric mean in child blood lead declined from 15.2 µg/dl in 1976–1980 to 0.8 µg/dl in 2011–2016.² However, these remarkable reductions were neither sufficient nor equitable, and significant racial inequalities in lead exposure remain evident not only in child blood lead records, but also in public drinking water records, as highlighted by Danzinger et al.¹ To eliminate these inequalities in lead exposure and improve child and adult health, investments in improving drinking water infrastructure are urgently needed across the United States. Persistent racial inequalities in lead exposure from regulated public drinking water systems are morally outrageous. Together, public health researchers and clinicians should advocate for the full elimination of drinking water lead exposure across the United States via nationwide infrastructure investments and regulatory changes.

Figure 1.

Timeline of major lead reduction regulations in the United States, 1971–2012. No other major lead regulation has been implemented nationwide since 2012. CDC, Centers for Disease Control and Prevention; OSHA, Occupational Safety and Health Administration.

Disclosures

All authors have nothing to disclose.

Funding

None.